Withdrawal: Reactive oxygen species (ROS) mediate p300-dependent STAT1 protein interaction with peroxisome proliferator-activated receptor (PPAR)-γ in CD36 protein expression and foam cell formation

Abstract

This article has been withdrawn by the authors. The authors and the journal conclude that the images between and within Figures 2D and 3D were reused. Specifically, the image “pcDNA” in Figure 3D was a duplication of the image “GW9662 + Vehicle” in Figure 2D. Similarly, the image “p300WT + 15(S)-HETE” in Figure 3D was captured from the well “PFS1YF + 15(S)-HETE” in Figure 2D. The image “p300WT” in Figure 3D was captured from the well “pcDNA + 15(S)-HETE” in Figure 3D itself. Additional potential internal reuse is in Figure 2D, STAT1(WT) + 15(S)-HETE” and Figure 2D, “PFS1YF + 15(S)-HETE”. The authors state that these image duplications do not affect the conclusions of the paper. The authors apologize for this oversight. Reactive Oxygen Species (ROS) Mediate p300-dependent STAT1 Protein Interaction with Peroxisome Proliferator-activated Receptor (PPAR)-γ in CD36 Protein Expression and Foam Cell FormationJournal of Biological ChemistryVol. 290Issue 51PreviewBackground: CD36 plays a role in lipid uptake, foam cell formation, and atherogenesis.Results: 15(S)-HETE induces CD36 expression and foam cell formation by triggering p300-mediated STAT1 acetylation and its interaction with PPARγ.Conclusion: STAT1 and PPARγ interact with each other in CD36 expression and foam cell formation.Significance: 15(S)-HETE appears to play an important role in foam cell formation, a critical event in atherogenesis. Full-Text PDF Open Access